Embodiments of the present invention pertain generally to methods and systems for measuring physiologic information utilizing an implantable cardiac patch for the early detection and prevention of congestive heart failure.
In the United States, it is estimated that approximately five million people have congestive heart failure (“CHF”). CHF is the inability of the heart to provide sufficient blood flow to meet the body's demand for oxygen. Patients suffering from CHF may also have associated cardiac diseases such as myocardial ischemia, which if prolonged lead to myocardial infarctions and life-threatening arrhythmias. Thus, it is desirable to be able to monitor and treat the local as well as global status of the heart.
A review of the cardiac conduction system is provided as background. A normal heartbeat occurs through an orderly deployment of electrical charge through the myocardium resulting in the contraction of the atrium followed by the contraction of the ventricles. The cardiac conduction system coordinates the depolarization of the heart. The heart includes a group of cells called the sinoatrial node (“SA node”), located in the atrium that initiate a heartbeat. Depolarization spreads radially through the atrium via atrial pathways to the atrioventricular node (“AV node”). Atrial depolarization may be complete in about 0.1 seconds. Propagation through the AV node takes place slowly to allow the atria to empty and the ventricles to fill with blood. This slow conduction in the AV node results in a delay (e.g. around 0.1 s) between atrial and ventricular excitation. When the depolarization arrives at the ventricles, a bundle of HIS spreads the excitation through the Purkinje system to the right and left ventricles at a relatively high velocity (e.g. 1-2 m/s). The wave of depolarization is rapidly conducted through the Purkinje fibers to all parts of the ventricles (e.g. in about 0.08-0.1 seconds). The timing of the heart's depolarization facilitates filling of the ventricles from atrial contraction prior to ventricular contraction. The cardiac conduction system provides the ability of the heart to have a rate and rhythm to provide the required blood flow to the body.
Myocardial Infarction (“MI”) occurs when the blood supply to parts of the myocardium is interrupted leading to the death of cardiac muscle cells. MIs are often complicated by serious arrhythmias. An arrhythmia occurs when a disease or an abnormality in the electrical pathway of the heart causes the normal cardiac rhythm, called sinus rhythm, to be disrupted. Patients with chronic myocardial infarction are at most risk of ventricular tachycardia (“VT”). Persistent VT leads to ventricular fibrillation (“VF”), where a part of the ventricular muscle fibers are depolarized and parts are completely repolarized. Multiple areas of the ventricles attempt to control the heart's rhythm resulting in the fibrillating ventricles inability to pump blood effectively. If not terminated and effectively treated, VF causes the blood circulation to stop, leading to cardiac arrest and death.
Standard medical treatments have been developed to treat heart disease. Historically, congestive heart failure has been managed by treating the patient with drugs, pacemakers and the like. Also, devices have been proposed to improve cardiac output such as left ventricular assist pumps and multi-chamber pacing to improve cardiac output. Electrocardiograms (“ECG”) have been used for detecting arrhythmias. In addition, cardiac harnesses have been employed to compress the heart and provide an electrical shock for defibrillation. Other devices such as implantable cardioverter defibrillators (ICDs) have been used to electrically shock the heart back to a normal cycle and to terminate most tachyarrhythmias, including atrial tachycardia (“AT”), VT and VF. An ICD typically has a lead from the ICD connected to the right ventricle and is used to detect both bradyarrhythmia and tachyarrhythmia. ICD therapy is usually prescribed to patients that have had one episode of VT/VF or suffered cardiac arrest. The ICD delivers an electric shock to depolarize the entire myocardium simultaneously in order to restore a normal rate and rhythm to the heart. One difficulty with current ICD therapies, especially in patients who have had an MI, is that there is no satisfactory method to reduce scar formation and myocardial wall thinning.
Recently, an epicardial mesh/patch has been proposed for use with the ICD that is inserted into the pericardial spaced and placed on the epicardium of the atrium or ventricle. The mesh/patch can be placed during open heart surgery or by minimally invasive intrapericardial lead placement techniques via the subxiphoid access. However, conventional epicardial mesh/patches are unable to detect deflections of the tissue as the heart is depolarized. Because of the anatomical difference of the atria and the ventricles, the sequential activation, depolarization, and repolarization of the atria and ventricles produce differentiable deflections. Thus, conventional ICDs are not able to detect an arrhythmia before it fully develops and similarly are unable to save cardiac tissue from being damaged. Furthermore, conventional implantable devices (e.g. ICD, pacemaker or otherwise) are unable to detect a MI in patients who have already suffered a MI.
A need remains, especially for patients who have recently suffered a myocardial infarction, for an implantable device that affords early detection of abnormal ventricular activation in order to prevent reentrant VT from occurring. This, in turn, may also prevent the occurrence of life-threatening VF that often follows VT.
A need remains for an improved cardiac patch that is directed to overcoming one or more of the problems set forth above. A need remains for an improved mesh/patch and implantable device having the ability to monitor myocardial deflections, sense abnormal heart rhythm, applying preventative pacing schemes during the early stages of MI, and measure the excitability of tissue and the tissue's response to various pacing schemes.